摘要
ARDS是一种以顽固低氧血症为主要特点的呼吸系统疾病,肺纤维化是ARDS公认的后遗症,但具体机制复杂。HMGB1作为一种晚期炎症因子可能是预防和治疗ARDS后肺纤维化的潜在靶点,可能机制与HMGB1诱导细胞如肺泡上皮-间质转分化、成纤维细胞、巨噬细胞等激活相关,涉及的通路可能有HMGB1/RAGE、HMGB1/TLR4通路等,本文旨在对HMGB1参与ARDS后肺纤维化的可能机制进行综述。
ARDS is a respiratory disease characterized by progressive dyspnea.Pulmonary fibrosis is a well-recognized sequelae of ARDS,but the specific mechanism is complex.HMGB1,as a late inflammatory factor,may be a potential target for the prevention and treatment of pulmonary fibrosis.The possible mechanism involve the activation of alveolar epithelial-mesenchymal transdifferentiation,fibroblasts and macrophages,and HMGB1/RAGE and HMGB1/TLR4 pathways might be involved in the process.This article aims to discuss the possible mechanism of HMGB1 involved in pulmonary fibrosis after ARDS.
作者
李磅
王红嫚
Li Pang;Wang Hongman(Department of Respiratory and Critical Care Medicine,the Fifth Affiliated Hospital of Zunyi Medical University,Zhuhai Guangdong 519100,China)
出处
《遵义医科大学学报》
2023年第7期725-730,共6页
Journal of Zunyi Medical University
基金
国家自然科学基金资助项目(NO:81960023)
贵州省卫生健康委科学技术基金资助项目(NO:kj2021-093)。
关键词
高迁移率族蛋白
急性呼吸窘迫综合征
肺纤维化
high mobility group protein B1
acute respiratory distress syndrome
pulmonary fibrosis
